Glycation of nutrient proteins and endogenous proteins in the presence of reducing sugars has been implicated in the pathogenesis of diseases such as Alzheimer's disease, neuropathy, nephropathy and retinopathy. Peroxidation of nutrient lipids and endogenous lipids has been implicated in the pathogenesis of diseases such as atherosclerosis and cancer. Together, glycated proteins and peroxidized lipids are called Advanced Glycation End-products (AGEs).
As shown in FIG. 1, amino acids/proteins react with reducing sugars to form glycated proteins. Cross links between proteins alters the proteins' structures and functions. Endogenously, this damages the extracellular matrix (ECM), basement membrane (BM) and smooth muscle tissue. Protein glycation also causing non-enzymatic browning in the nutrient proteins.
Protein glycation reactions are called Maillard Reaction. Here are the various stages of protein glycation:
In phase 1, schiff base is formed from the condensation of an amine group with the carbonyl group of a reducing sugar's aldehyde or ketone. The result is a Schiff base, an imine, in which C═O is replaced by C═N. An Amadori product is a re-arrangement from the Schiff base, in which the hydrogen atom from the OH adjacent to C═N moves to bond to nitrogen.
In phase 2, the Amadori products undergo any of these:                a. Dehydration forms reductones and dehydro reductones, which form carboxymethyl lysine and hydroxymethyl furfural.        b. Strecker degradation: Amadori products undergo enolization and deamination to produce dicarbonyls, which undergo decarboxilation and hydrolysis to produce a Strecker aldehyde.        c. Losing three water molecules and reacting with amino acids and water yields furfural and hydroxymethyl furfural.        
In the third phase, phase 2 products react with amino acids to form melanoidins, precursors to the formation of glycated proteins.
FIG. 2 shows the oxidative degradation of lipids by reactive oxygen species (ROS). Here are the main steps of lipid peroxidation reactions.
Initiation: A fatty acid radical is produced. An ROS attacks the fatty acid, causing a hydrogen atom to be extracted from a methylene group. This generates fatty acid radicals.
Propagation:                a. The fatty acid radical reacts with molecular oxygen and produces a peroxyl-fatty acid radical.        b. The peroxyl-fatty acid radical reacts with a methylene group in the lipid and produces a lipid hydroperoxide and fatty acid radical.        c. The unstable lipid hydroperoxide breaks to produce alkoxy and a hydroxyl radical.        d. The alkoxy reacts with another methylene group and produces an alcohol and fatty acid radical.        e. These steps repeat.        
Termination:                a. The fatty acid radical reacts with molecular oxygen and produces a peroxyl-fatty acid radical.        b. Two alkoxy radicals react to produce lipid peroxide.        c. A peroxyl-fatty acid radical reacts with a fatty acid radical to form lipid peroxide.        d. An alkoxy radical reacts with a fatty acid radical to produce ether.        e. Two peroxyl-fatty acid radicals react to produce lipid peroxide and molecular oxygen.        
Methods for inhibiting glycation of nutrient and endogenous proteins and peroxidation of nutrient and endogenous lipids are needed to provide a cure for major diseases.